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Experimental Protocol for Detecting Mitochondrial Function in Hepatocytes Exposed to Organochlorine Pesticides
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Experimental Protocol for Detecting Mitochondrial Function in Hepatocytes Exposed to Organochlorine Pesticides

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2, 2', 4, 4'-tetrabromodiphenyl ether (BDE-47) induces mitochondrial dysfunction and related liver injury via

Feng Chen1, Li Feng1, Yuan-Lin Zheng1

  • 1School of Life Science, Jiangsu Normal University, Xuzhou, 221116, Jiangsu Province, PR China; Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, Jiangsu Normal University, Xuzhou, 221116, Jiangsu Province, PR China; College of Health Science, Jiangsu Normal University, Xuzhou, 221116, Jiangsu Province, PR China.

Environmental Pollution (Barking, Essex : 1987)
|December 16, 2019
PubMed

Insights

2,2

Area of Science:

  • Environmental toxicology
  • Cellular biology
  • Molecular mechanisms of liver injury

Background:

  • 2,2',4,4'-Tetrabromodiphenyl ether (BDE-47) is linked to adverse health outcomes, but its toxicity mechanisms remain unclear.
  • Mitochondrial injury and mitophagy impairment are implicated in BDE-47-induced liver damage.
  • Understanding BDE-47's impact on mitophagy is crucial for assessing its hepatotoxicity.

Purpose of the Study:

  • To investigate if BDE-47 impairs mitophagy, leading to mitochondrial dysfunction and liver injury.
  • To elucidate the underlying molecular mechanisms, including the role of NAD+ and specific signaling pathways.
  • To explore the involvement of miR-34a-5p in BDE-47-induced hepatotoxicity.

Main Methods:

  • In vivo mouse models exposed to BDE-47.
  • Analysis of mitochondrial function, mitophagy markers, and oxidative stress.
  • Investigation of NAD+ levels, Sirt3/FoxO3a/PINK1 signaling pathway.
  • Assessment of miR-34a-5p expression and its targeting of NAMPT using AAV-sponge and luciferase assays.

Main Results:

  • BDE-47 exposure caused mitochondrial dysfunction and oxidative liver injury by impairing mitophagy.
  • NAD+ insufficiency was identified as a key factor in BDE-47-induced mitophagy defects and mitochondrial dysfunction.
  • BDE-47 upregulated miR-34a-5p, which suppressed NAMPT, reduced NAD+, and inhibited Sirt3/FoxO3a/PINK1 signaling, thereby impairing mitophagy.

Conclusions:

  • BDE-47 induces mitochondrial dysfunction and liver injury through mitophagy impairment.
  • The miR-34a-5p/NAMPT/NAD+ axis plays a critical role in BDE-47-mediated hepatotoxicity.
  • Targeting miR-34a-5p-mediated mitophagy impairment offers a potential therapeutic strategy for BDE-47 toxicity.
Keywords:
Liver injuryMitochondriaNAD(+)Polybrominated diphenyl ethersmiRNA

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